The irritating nature of poison ivy sap was first recorded in 1609 by Captain John Smith after his arrival in North America. Since that time many compounds and practices have been tried unsuccessfully to mitigate, render harmless, or destroy, the toxic principle of the dermatogenic members of the botanical family Anacardiaceae. The members, which include poison ivy, poison oak, poison sumac, the lacquer tree, mango and cashew, belong to an immunologic cross reacting group which have biochemically similar antigens. The antigens are 1,2 dihydroxy-benzenes with a 15 or 17 carbon atom aliphatic side chain which has varying degrees of unsaturation. It is not unusual for the sap of different plants to have mixtures of dihydroxy benzenes or to have these compounds in common but at different concentration levels.
The allergic contact dermatitis is reported in the literature to be caused by the catechol moiety as the primary allergen. The aliphatic hydrocarbon side group allows bonding to and penetration of the skin.
Exposure of skin to the urushiol, after a time, results in a painful rash and itching at the area of contact which often proceeds to vesicles. The dermatological reaction may require a month or more to heal.
Bare skin contact with the urushiol is a prerequisite for the allergic reaction. However, direct contact with the plant sap by bare skin is not necessary and often is not the primary contamination surface. In fact, there are many vectors responsible for the spread of the urushiol; for example, clothing, tools, and domestic animals, and even the fingers spread the urushiol to other parts of the body. Failure to appreciate an exposed article as a carrier is responsible for most personal exposure. Evading this secondary contamination from exposed articles is difficult because of the small amount of the urushiol needed to cause the allergic reaction as well as the relatively unobtrusive evidence of its presence. Furthermore, even if exposure of skin or articles were noted, this most often would occur in the field where there is usually no access to relief, such as clean clothes or the ability to scrub with soap and water. Additionally, contaminated articles can retain allergic reaction-causing capabilities for up to one year after the original exposure because of the refractory nature of the urushiol oleoresin.
It might seem relatively easy to destroy the urushiol since the catechol moiety is a strong reducing agent and might be expected to react readily with strong oxidizing agents to accomplish its destruction. This is the case when acidic, aqueous solutions of strong oxidizers such as permanganates, peroxides, or chlorites effectively destroy the catechol as the water soluble pyrocatechol. However, these same oxidizing agents will not destroy the hydrophobic catechol moiety as presented in the urushiol.